Measurement of DNA damage with endonucleases, which recognize lesions such as pyrimidine dimers or ionizing radiation base damage, has been used to study DNA repair in mammalian cells. The sensitivity of this approach has been increased 1 to 2 orders of magnitude by adapting it to the alkaline elution technique. We have adapted this technique to quantitatively measure very low levels of base damage produced by x-rays in various human cell strains. We have found that ataxia telangiectasia (AT) cells, which are hypersensitive to x-rays, remove this base damage normally after doses of 1 to 5 k rads. This is in contrast to Patterson's findings at higher x-ray doses where some AT cells, but not other AT cells, removed the base damage slower than normal. We conclude that the cause for the x-ray hypersensitivity in AT cells does not involve base damage or its repair. We have also studied the repair of x-ray base damage in xeroderma pigmentosum (XP) cells. Cells from patients with this disorder are hypersensitive to UV-radiation and are deficient in the repair of DNA base damage, pyrimidine dimers, produced by UV; some XP cells rare also moderately hypersensitive to x-rays. We found that most , greater than 90%, of x-ray base damage is repaired in XP cells, but the remaining persists in all XP cell strains tested, complementation groups A, C, D, and G. This abnomality in DNA repair did not correlate with x-ray hypersensitivity. It is likely that the persistent base damage seen in XP cells are pyrimidine dimers since a very low level would be expected to be produced by Cerenkov radiation during x-irradiation.